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Study of the Uterine Local Immune Response in a Murine Model of Embryonic Death Due to Tritrichomonas foetus

Authors

  • Mariana A. Woudwyk,

    1. Laboratory of Histology and Embryology, Faculty of Veterinary Sciences, National University of La Plata, La Plata, Buenos Aires, Argentina
    2. Experimental Obstetrics & Gynecology, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany
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  • Cristina E. Monteavaro,

    1. Laboratory of Clinical and Experimental Microbiology, Faculty of Veterinary Sciences, National University of the Center of Buenos Aires Province, Tandil, Buenos Aires, Argentina
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  • Federico Jensen,

    Corresponding author
    • Experimental Obstetrics & Gynecology, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany
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  • Pedro Soto,

    1. Laboratory of Clinical and Experimental Microbiology, Faculty of Veterinary Sciences, National University of the Center of Buenos Aires Province, Tandil, Buenos Aires, Argentina
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  • Claudio G. Barbeito,

    1. Laboratory of Histology and Embryology, Faculty of Veterinary Sciences, National University of La Plata, La Plata, Buenos Aires, Argentina
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    • ACZ and CGB share senior authorship.

  • Ana C. Zenclussen

    1. Experimental Obstetrics & Gynecology, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany
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    • ACZ and CGB share senior authorship.


Correspondence

Federico Jensen, Experimental Obstetrics & Gynecology, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany.

E-mail: federico.jensen@med.ovgu.de

Abstract

Problem

Bovine tritrichomonosis is a sexually transmitted disease caused by Tritrichomonas foetus, characterized by conceptus loss. We developed a mouse model of tritrichomonosis to study the mechanisms involved in the embryonic death. We hypothesized that embryonic death may be due to an exacerbated maternal response to the pathogen that then affects embryo development.

Method of study

We infected BALB/c mice with Tritrichomonas foetus and paired them after confirming active infection. We studied the expression of pro- and anti-inflammatory cytokines, markers for T regulatory and T helper 17 cells as well as haem-oxygenase-1 expression in uterine tissue by real-time RT-PCR.

Results

As expected, TNF-α was augmented in infected animals. IL-10 and IL-4 were also up-regulated. Treg-associated genes were higher expressed in uteri of infected group. In mice that have lost their conceptus after the infection, haem-oxygenase-1 (HO-1) mRNA levels were strongly decreased, while RORγt mRNA, a reliable marker for Th17, was augmented in uterus.

Conclusion

A T effector response of type 1 and 17 may be involved in tritrichomonosis-related embryonic death. This alters protective mechanisms as HO-1. Increased regulatory T cells may facilitate embryonic death by promoting the persistence of infection.

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